4. Important clinically because:
1)acute severe hyponatremia can cause substantial
morbidity and mortality;
2)adverse outcomes are higher in hyponatremic
patients with a wide range of underlying diseases;
3)overly rapid correction of chronic hyponatremia can
cause severe neurological deficits and death.
12. A defect in osmoregulation causes vasopressin to be
inappropriately stimulated, leading to urinary concentration.
MCC of euvolumic hyponatremia
Excess vasopressin: CNS disturbances such as hemorrhage,
tumors, infections, and trauma.
Ectopic vasopressin: Small cell lung cancers, cancer of the
duodenum and pancreas, and olfactory neuroblastoma.
Idiopathic: seen in elderly(10%).
SIADH (Syndrome of Inappropriate ADH Secretion)
13. Is a syndrome described following SAH, head injury, or
neurosurgical procedures, as well in other settings.
Primary defect is salt wasting from the kidneys(?role of
BNP) with subsequent volume contraction, which
stimulates vasopressin release.
Uncommon.
Cerebral Salt Wasting
syndrome
15. Criteria for Diagnosing SIADH
Decreased effective osmolality of the extracellular fluid.
Inappropriate urinary concentration (Uosm >100 mOsmol/kg
H2O) with normal renal function) at some level of plasma hypo-
osmolality.
Clinical euvolemia.
Elevated urinary sodium excretion (>20 mmol/L) while on
normal salt and water intake.
Absence of other potential causes of euvolemic hypo-osmolality
Normal renal function and absence of diuretic use, particularly
thiazide diuretics.
23. Treatment
When considering the treatment of patients with
hyponatremia, five issues must be addressed:
• Risk of osmotic demyelination
Appropriate rate of correction to minimize this risk
•
•
•
•
•
Optimal method of raising the plasma sodium
concentration
Estimation of the sodium deficit if sodium is to be
given
Management of the patient in whom overly rapid
correction has occurred
24. General principles of treatment
.Primarily determined by the severity of symptoms and
the cause of the hyponatremia
• Symptomatic hyponatremia (seizures, or coma)
o likely to occur with an acute case andmarked
reduction in the plasma sodium concentration
o Aggressive therapy is required.
o Chronic but significant hyponatremia
where less severe neurologic symptoms occur
fatigue, nausea, dizziness, gait disturbances,
confusion, lethargy, and muscle cramps
These symptoms typically do not mandate
aggressive therapy
25. Methods of Sodium Correction
• Water restriction
• primary therapy for hyponatremia in edematous states,
SIADH, primary polydipsia, and advanced renal failure.
• Sodium chloride administration
•
• usually as isotonic saline or increased dietary salt
given to patients with true volume depletion, adrenal
insufficiency, and in some cases of SIADH.
contraindicated in edematous patients (eg, heart
failure, cirrhosis, renal failure) since it will lead to
exacerbation of the edema
•Hypertonic saline is generally recommended only for
patients with symptomatic or severe hyponatremia.
26. • The increase in plasma Na+concentration can be highly
unpredictable during treatment with hypertonic saline due
to rapid changes in the underlying physiology.
• Patient should be monitored carefully for changes in
neurologic and pulmonary status, and serum electrolytes
should be checked frequently, every 2 - 4 hours.
27. Goal:
Urgent correction by 1-2 mmol/hr upto 4-8mmol/L / 24
hours, to prevent brain herniation and neurological
damage from cerebral ischemia.
Upper limit for correction,10-12 mmol/L in any 24hour
period; 18 mmol/L in any 48-hour period.
Treatment of symptomatic acute hyponatremia
28. how much fluids to give?
Total body water = weight x 0.6 for men / 0.5 for woman
• One liter of NS contains: 154 mmol/L of Na+ Cl−
• One liter of 3% saline contains:513 mmol/L of Na+ Cl−
29. Example: An 60-kgmanishavingseizure.His s.Nais110
mmol/L.
Means of correction:
Given theacuity,thepatientshouldbegivenhypertonic saline,
which has513mmolofNaperliter.
{513- 110} /{60 x 0.6+1}= 10mmol/L
One liter of thisfluid would increaseNaby 10mmol/L.
Doseof hypertonic salineat200mL/hr until symptoms
improve. Maximum1litre of 3% NSshouldbegivenin 24
hour.
30. Goal:
lower goal of
4-8 mmol/L/24 hours
4-6 mmol/L per day if the risk of ODS is high.
Limits not to exceed:
• 8-10 mmol/L in any 24-hour period.
Treatment of chronic hyponatremia(Avoiding
ODS)
31. Treatment of hypovolemic hyponatremia
Diuretic related- Discontinuation of thiazides and
correction of volume deficits.
Mineralocorticoid deficiency- Volume repletion with
isotonic saline, Fludrocortisone chronically for
mineralocorticoid replacement.
32. SIADH - For most cases of mild-to moderate SIADH, fluid
restriction represents the cheapest and least toxic therapy. (fluid
restriction 500 mL/d below the 24-hour urine volume.
Failure to water restriction
- Vaptans
- Democlocycline 150- 300 mg PO tid or qid
-Fludrocortisone 0.05-0.2 mg bid
Treatment of euvolemic hyponatremia
33. Glucocorticoid Deficiency-glucocorticoid replacement
at either maintenance or stress doses, depending on
the degree of intercurrent illness.
Severe Hypothyroidism-thyroid hormone replacement at
standard weight-based doses; several days may be needed
to normalize the serum [Na].
34. Heart Failure-for patients with mild to moderate
symptoms, begin with fluid restriction (1 L/d total) and, if
signs of volume overload are present, administer loop
diuretics.
If the serum [Na] does not correct to the desired level,
consider lifting the fluid restriction and vaptans
Treatment of hypervolemic
hyponatremia
35. Cirrhosis-Severe daily fluid restriction,
Vaptans an alternative choice if fluid restriction has failed to maintain
a serum [Na] 130 mmol/L; however, tolvaptan use should be
restricted to cases where the potential clinical benefit outweighs the
risk of worsened liver function, such as in patients with end-stage
liver disease and severe hyponatremia who are awaiting imminent
liver transplantation.
36. CKD-Restricting fluid intake. Aquaretics (vaptans)
can be employed{not be expected to cause a
clinically significant aquaresis with severe renal
impairment (ie, serum creatinine >220
mmoL/l)}.
37. Role of VAPTANS
Vaptans have long been anticipated as a more effective
method to treat hyponatremia by virtue of their unique effect
to selectively increase solute-free water excretion by the
kidneys.
Although not C/I with decreased renal function, these
agents generally will not be effective if S.Cr is >220.
39. ODS occurs if chronic hyponatremia is corrected too
rapidly.
Present in a stereotypical biphasic pattern (initially
improve neurologically with correction of hyponatremia,
but then, one to several days later, new, progressive, and
sometimes permanent neurological deficits emerge).
40. • Patients can present para- or quadraparesis, dysphagia,
dysarthria, diplopia, a "locked-in syndrome," and/or loss of
consciousness.
• Most commonly affected area is pons.
• Other regions of the brain affected in ODS: (in order of
frequency) cerebellum, lateral geniculate body, thalamus,
putamen, and cerebral cortex or subcortex.
41. • As these lesions may not appear until 2 weeks after development, a diagnosis
of myelinolysis should not be excluded if the imaging is initially normal.
42. Starting serum [Na] ≥120 mmol/L: Intervention unnecessary.
Starting serum [Na] <120 mmol/L:
Withhold the next dose of vaptan if the correction is >8
mmol/L;
Consider therapeutic re-lowering of serum [Na] if
correction exceeds therapeutic limits;
Consider administration of high-dose glucocorticoids (eg,
dexamethasone, 4 mg every 6 hrs) for 24-48hrs following
the excessive correction.
Managing excessive correction of chronic hyponatremia
43. Re-lowering serum [Na]:
Administer desmopressin to prevent further water losses:
2-4 mg every 8 hours parenterally;
Replace water orally or as 5% dextrose in water
intravenously: 3 mL/kg/h;
Recheck serum [Na] hourly and continue therapy infusion
until serum [Na] is reduced to goal
